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ADC Online First, published on June 23, 2010 as 10.1136/adc.2009.175927

Original article

Fatness leads to inactivity, but inactivity does not

lead to fatness: a longitudinal study in children
(EarlyBird 45)
B S Metcalf,1 J Hosking,1 A N Jeffery,1 L D Voss,1 W Henley,2 T J Wilkin1
1Department

of Endocrinology
and Metabolism, Peninsula
Medical School, Plymouth, UK
2Department of Mathematics
and Statistics, University of
Plymouth, Plymouth, UK
Correspondence to
Brad S Metcalf, Department
of Endocrinology
and Metabolism,
Peninsula Medical School,
University Medicine, Level 7,
Derriford Hospital,
Plymouth PL6 8DH, UK;
brad.metcalf@phnt.swest.
nhs.uk
Accepted 26 April 2010

ABSTRACT
Objective To establish in children whether inactivity is
the cause of fatness or fatness the cause of inactivity.
Design A non-intervention prospective cohort study
examining children annually from 7 to 10 years. Baseline
versus change to follow-up associations were used to
examine the direction of causality.
Setting Plymouth, England.
Participants 202 children (53% boys, 25% overweight/
obese) recruited from 40 Plymouth primary schools as
part of the EarlyBird study.
Main outcome measures Physical activity (PA) was
measured using Actigraph accelerometers. The children
wore the accelerometers for 7 consecutive days at
each annual time point. Two components of PA were
analysed: the total volume of PA and the time spent at
moderate and vigorous intensities. Body fat per cent
(BF%) was measured annually by dual energy x ray
absorptiometry.
Results BF% was predictive of changes in PA over the
following 3 years, but PA levels were not predictive of
subsequent changes in BF% over the same follow-up
period. Accordingly, a 10% higher BF% at age 7 years
predicted a relative decrease in daily moderate and
vigorous intensities of 4 min from age 7 to 10 years
(r=0.17, p=0.02), yet more PA at 7 years did not
predict a relative decrease in BF% between 7 and
10 years (r=0.01, p=0.8).
Conclusions Physical inactivity appears to be the
result of fatness rather than its cause. This reverse
causality may explain why attempts to tackle
childhood obesity by promoting PA have been largely
unsuccessful.

The prevalence of childhood overweight/obesity

is increasing annually in many developed and
developing countries,1 reaching approximately
30% in the UK and the USA by 2004. 2 3 Childhood
overweight/obesity is of concern because it may
be a precursor to serious health complications
(eg, diabetes, cardiovascular disease, metabolic
disturbance) later in life.4 Type 2 diabetes, which
a generation ago seldom emerged before middle
age, is increasingly a disease of adolescence and
childhood. 5
The cause of obesity is multifactorial but results,
in the main, from a chronic imbalance between
energy intake and energy expenditure (basal/
resting, physical activity (PA) and thermogenic
response to feeding). PA accounts for 25%35%
of total energy expenditure in children 6 and is
deemed important because it is potentially modi able. The widely held belief is that inactivity

What is already known on this topic

It is widely believed from cross-sectional

studies that childhood obesity is caused by
physical inactivity.
Direction of causality cannot be inferred from
cross-sectional associations, their findings
could equally represent obesity leading to
physical inactivity.
Public health and school-based interventions
designed to make children more active rarely
succeed in reducing obesity.

What this study adds

Physical inactivity is the result rather than the

cause of obesity.
The relationship between fatness and PA is
dominated by the impact of fatness on activity
and not at all by activity on fatness.
This reverse causality may explain why PA
interventions so often fail to prevent excess
weight gain in children.

leads to fatness, and this is reected in a series of

public health initiatives aimed at making children
more active. The UK government has recently
published guidelines on PA in preschool and
school-aged children 7 and is currently promoting
Change4Life, a campaign that encourages families to adopt a more active lifestyle.8
Although there is overwhelming evidence that
PA and obesity are linked, observational and
experimental data do not always agree. Thus,
two large and well-established European observational studies reported inverse associations
(r0.20) between objectively measured PA and
body fat per cent (BF%),9 10 whereas only 3 of 11
intervention trials reviewed by Wareham and
colleagues11 showed even a modest impact of PA
on body composition. The authors of the observational studies both conceded that their crosssectional design could not infer the direction of
causality, yet both interpreted their ndings as
inactivity leads to fatness. One explanation
for the inconsistency between observational and
experimental ndings could be reverse causality.

Metcalf BS,
Hosking J,author
Jeffery AN,
et al.
Arch Dis
Child (2010). doi:10.1136/adc.2009.175927
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Original article
The cross-sectional correlations could equally well mean
that fatness leads to inactivity, in which case PA intervention
would not be expected to affect body mass.
Cause must precede effect, and longitudinal studies that
measure fatness and activity levels at baseline and long-term
follow-up can use the rule of temporality to investigate the
dominant direction of causality. Four studies have carried out
this kind of analysis in adults,1215 but none has done so in
children. All four adult studies reported a signicant inverse
association between baseline fatness and follow-up PA but not
between baseline PA and follow-up fatness, suggesting that
fatness leads to inactivity but that inactivity does not lead to
fatness. The aim of the present study was to use the rule of
temporality to elucidate the dominant direction of causality
between objective measures of PA and BF% in children.

METHODS
Design, setting and participants
The EarlyBird study is a non-intervention prospective cohort
study investigating the factors that lead to childhood obesity
and its associated metabolic disturbances. Some 307 healthy
children (55% boys, 98% Caucasian) were recruited at school
entry (aged 5 years) between January 2000 and January 2001
from 54 Plymouth primary schools, randomised to ensure a
socio-economic mix representative of the city and of the UK
in general (index of multiple deprivation 2004 score: EarlyBird
cohort 26.1, Plymouth 26.3 and England 21.7 with cities ranging from 8 to 45).16 The studys rationale, recruitment procedures and protocol have been reported in detail elsewhere.17
The exclusion criteria included diabetes, pathologic conditions likely to affect growth or body composition, moderate
or severe physical disability and long-term use of oral steroids.
The cohort is measured annually, and this report covers four
annual time points from age 7 years (when BF% was rst
measured objectively) to age 10 years. The mean age at each
time point is narrow (SD 3 months), deemed important for
the resolution of age-related events, and the follow-up interval
was 1.0 year (SD 1 month). Local research ethics committee
approval was obtained in 1999.

Measures
Physical activity
PA was measured objectively on four annual occasions using
Actigraph accelerometers (formerly MTI/CSA, Fort Walton
Beach, Florida, USA). Children were asked to wear the accelerometers for 7 consecutive days (5 school days and 2 weekend days) at each annual time point, and only recordings that
captured at least 5 days (including 1 weekend day) were used.
The Actigraph records the intensity of movement every onetenth of a second, and for this study, the counts were collected
into epochs of 1 min and stored against clock time. The parents were asked to record periods when their child removed
the accelerometer during waking time, so that false periods
of inactivity could be identied. False periods were replaced
with the mean accelerometer counts recorded at the same
clock time on the other days. Total PA (counts per week) and
time spent in moderate and vigorous PA (MVPA, minutes per
day) were analysed. Actigraphs have been shown to correlate well with free-living measures of energy expenditure in
children (r=0.70 independent of body weight18; r=0.92 with
body weight19), and their technical reproducibility is impressive (between-Actigraph coefcient of variability 5%; withinActigraph coefcient of variability <2%). 20 The sensitivity of
2 of 6

each accelerometer was measured under controlled conditions

by a motorised turntable. 20 Seasonality was measured on a
continuous scale by the number of relevant daylight hours
(between 08:00 and 21:00) specic to Plymouth for the week
the accelerometer was worn. 21

Body fat
Whole BF% was measured by dual energy x ray absorptiometry (DEXA; Lunar Expert, Lunar, Madison, New York,
USA), considered to be a criterion method for measuring body
composition. 22 Body mass index (BMI, kilogram per meter
squared) and waist circumference (WC) were also measured
and expressed as age- and sex-specic SD scores (BMI-SDS and
WC-SDS) using the 1990 UK reference data.

Sample size
Of the 278, 269, 265 and 259 children who attended the
appointments at age 7, 8, 9 and 10 years, respectively, 238,
230, 229 and 225, respectively, had measures of PA and BF%.
To maximise sample comparability, this report is based on the
202 children (107 boys and 95 girls) for whom measures of PA
and BF% were obtained at all four time points.

STATISTICS
All data analyses were carried out using SPSS V.15. Cohort
characteristics were summarised by the means and SD for
each sex at each annual time point, except for BF% that was
positively skewed and expressed as the median and the interquartile range. Each annual sample of PA (total PA and MVPA)
was adjusted for seasonality and the sensitivity of the accelerometers using the respective regression coefcients obtained
when modelling PA.
Multiple linear regression modelling was performed to
quantify the association between PA and the measures of
BF% cross sectionally at each annual time point, 7, 8, 9 and
10 years, adjusted for age and sex (eg, PA 7y=Sex+Age7y+BF%7y).
The residuals generated from the models did not violate the
assumptions of multiple linear regression modelling. The same
method was used to establish the time-lagged association of
PA on future BF% measured 1, 2 and 3 years later and, the
reverse, BF% on future PA measured 1, 2 and 3 years later (eg,
PA10y=Sex+Age7y+BF%7y). 23
Changes in PA and BF% were calculated for each child over
each 1-, 2- and 3-year period. Multiple regression modelling was
then performed to quantify the association between the predictor at a single time point and the change in the outcome variable from that time point to a 1-, 2- or 3-year follow-up. These
models were adjusted for the outcome measure at the earlier
time-point (eg, PA10yPA 7y=Sex+Age7y+PA 7y+BF%7y).23

RESULTS
Trends
Girls had higher BMI-SDS, WC-SDS and BF% than boys and
were less physically active (table 1). In both sexes, BMI-SDS,
WC-SDS and BF% increased with age and PA (total and MVPA)
decreased with age.

Associations (cross sectional)

Whereas measures of fatness and PA differed between the
sexes, the strength of association between the variables did
not (sex interactions: all p>0.2). Consequently, all associations
(cross sectional, time lagged and change in outcome) were
derived from boys and girls together with adjustment for sex.
The cross-sectional correlations between BF% and PA were

Metcalf BS, Hosking J, Jeffery AN, et al. Arch Dis Child (2010). doi:10.1136/adc.2009.175927

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Original article
similar for total PA (r=0.18 to 0.23) and MVPA (r=0.20 to
0.25) at all ages (tables 2 and 3). The cross-sectional correlations were slightly lower for BMI-SDS versus PA (eg, MVPA:
r=0.12 to 0.18) and WC-SDS versus PA (eg, MVPA: r=0.10
to 0.22).

Table 1

Associations (time lagged)

Simple time-lagged correlations of BF% versus future PA were
slightly, though not signicantly, stronger than the correlations for PA versus future BF% when the time lag was 1 year
(eg, MVPA: r=0.27 vs 0.19), 2 years (r=0.22 vs 0.20) and

Summary characteristics by age and sex (mean (SD))

Visit

Sex

Variable

7 years

8 years

9 years

10 years

Boys (n=107)

Age (years)
BMI (SD score)
WC (SD score)
Body fat (%)
Total PA (counts105/week)
MVPA (min/day)
Age (years)
BMI (SD score)
WC (SD score)
Body fat (%)
Total PA (counts105/week)
MVPA (min/day)

6.89 (0.26)
0.21 (1.09)
0.19 (1.04)
13.0 (7.4)
38.7 (8.3)
56.9 (22.6)
6.88 (0.25)
0.58 (1.05)
0.48 (1.14)
20.0 (11.9)
34.3 (6.3)
44.5 (15.5)

7.85 (0.28)
0.30 (1.14)
0.36 (1.09)
13.6 (8.8)
38.7 (8.4)
57.3 (21.5)
7.82 (0.29)
0.61 (1.12)
0.53 (1.20)
21.4 (14.5)
33.9 (7.8)
43.7 (18.0)

8.87 (0.28)
0.38 (1.13)
0.45 (1.10)
16.0 (12.0)
37.8 (8.0)
56.5 (19.6)
8.84 (0.29)
0.70 (1.10)
0.74 (1.23)
25.6 (13.4)
33.6 (7.3)
41.9 (16.9)

9.91 (0.29)
0.44 (1.14)
0.58 (1.06)
18.8 (15.3)
35.8 (9.4)
52.3 (24.1)
9.87 (0.28)
0.73 (1.17)
0.87 (1.27)
27.0 (14.0)
32.0 (7.1)
37.6 (13.8)

Girls (n=95)

Median (interquartile range).

BMI, body mass index; PA, physical activity; MV, moderate-and-vigorous; SD, standard deviation; WC, waist circumference.

Table 2 Correlations between total PA and BF% (cross sectional and

time lagged by 1, 2 and 3 years), partial r (95% CI)

Table 3 Correlations between MVPA and BF% (cross sectional and

time lagged by 1, 2 and 3 years), partial r (95% CI)

Cross sectional (years)

Cross sectional (years)

TPA vs BF%

MVPA vs BF%

7 vs 7
8 vs 8
9 vs 9
10 vs 10

0.22 (0.35 to 0.08)*

0.20 (0.33 to 0.06)*
0.18 (0.31 to 0.04)**
0.23 (0.36 to 0.09)***

Time-lagged (years)

TPA vs future BF%

7 vs 8
8 vs 9
9 vs 10
7 vs 9
8 vs 10
7 vs 10

0.17 (0.30 to 0.03)**

0.20 (0.33 to 0.06)*
0.12 (0.25 to +0.02)
0.14 (0.27 to 0.00)**
0.17 (0.30 to 0.03)**
0.16 (0.29 to 0.02)**

7 vs 7
8 vs 8
9 vs 9
10 vs 10

0.22 (0.35 to 0.08)**

0.23 (0.36 to 0.09)***
0.20 (0.33 to 0.06)**
0.25 (0.38 to 0.12)***

BF% vs future TPA

Time lagged (years)

MVPA vs future BF%

BF% vs future MVPA

0.24 (0.37 to 0.10)***

0.17 (0.30 to 0.03)**
0.26 (0.38 to 0.13)***
0.18 (0.31 to 0.04)**
0.20 (0.33 to 0.06)*
0.21 (0.34 to 0.07)*

7 vs 8
8 vs 9
9 vs 10
7 vs 9
8 vs 10
7 vs 10

0.16 (0.29 to 0.02)*

0.23 (0.36 to 0.09)***
0.17 (0.30 to 0.03)*
0.18 (0.31 to 0.04)*
0.23 (0.36 to 0.09)**
0.15 (0.28 to 0.01)*

0.31 (0.43 to 0.18)***

0.21 (0.34 to 0.07)**
0.29 (0.41 to 0.16)***
0.20 (0.33 to 0.06)**
0.24 (0.37 to 0.10)***
0.25 (0.38 to 0.12)***

All correlations in this table are partial correlations controlled for sex and age.
n=202 for all analyses.
*p<0.05, **p<0.01,***p<0.001.
BF%, body fat%; TPA, total physical activity.

All correlations in this table are partial correlations controlled for sex and age.
n=202 for all analyses.
*p<0.05, **p<0.01,***p<0.001.
BF%, body fat%; MVPA, moderate-and-vigorous physical activity.

Table 4 Correlations of total PA versus change in BF% and BF% versus change in total PA, partial r (95% CI)

Table 5 Correlations of MVPA versus change in BF% and BF% versus

change in MVPA, partial r (95% CI)

Change in outcome
(years)

TPA vs change in BF%

BF% vs change in TPA

Change in outcome
(years)

MVPA vs change in BF%

BF% vs change in MVPA

7 vs 78
8 vs 89
9 vs 910
7 vs 79
8 vs 810
7 vs 710

+0.01 (0.13 to +0.15)

0.09 (0.23 to +0.05)
+0.09 (0.05 to +0.23)
0.02 (0.16 to +0.12)
0.06 (0.20 to +0.08)
0.05 (0.19 to +0.09)

0.16 (0.29 to 0.02)*

0.09 (0.23 to +0.05)
0.20 (0.33 to 0.06)**
0.07 (0.21 to +0.07)
0.10 (0.23 to +0.04)
0.13 (0.26 to +0.01)

7 vs 78
8 vs 89
9 vs 910
7 vs 79
8 vs 810
7 vs 710

+0.07 (0.07 to +0.21)

0.05 (0.19 to +0.09)
0.01 (0.15 to +0.13)
+0.01 (0.13 to +0.15)
0.04 (0.18 to +0.10)
0.01 (0.15 to +0.13)

0.20 (0.33 to 0.06)*

0.13 (0.26 to +0.01)
0.22 (0.35 to 0.08)*
0.13 (0.26 to +0.01)
0.16 (0.29 to 0.02)**
0.17 (0.30 to 0.03)**

All correlations in this table are partial correlations controlled for sex, age and
the outcome variable obtained at the same time-point as the predictor variable.
n=202 for all analyses.
*p<0.05, **p<0.01.
= change; BF%, body fat%; TPA, total physical activity.

All correlations in this table are partial correlations controlled for sex, age and
the outcome variable obtained at the same time-point as the predictor variable.
n=202 for all analyses.
*p<0.05, **p<0.01.
= change, BF%, body fat%; MVPA, moderate-and-vigorous physical activity.

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3 years (r=0.25 vs 0.15) and were of similar strength to the
cross-sectional correlations (table 2).

Associations (change in outcome)

There were no signicant associations between PA and subsequent change in BF%, yet for the reverse analysis, BF% versus
changes in PA, half the associations were small to moderate, ranging from r=0.16 to 0.22 and statistically signicant (tables 4 and 5). Using the longest follow-up period as an
example, BF% at 7 years predicted change in MVPA from 7
to 10 years (r=0.17, p=0.02), but MVPA at 7 years did not
predict change in BF% from 7 to 10 years (r=0.01, p=0.8).
The slope coefcients obtained from the change in the MVPA
model indicated that an additional 10% BF% at age 7 years
results in a relative decrease in daily MVPA of 4 min from
age 7 to 10 years (p=0.02). The equivalent change in outcome
associations that used BMI-SDS and WC-SDS in place of BF%
were weaker and not signicant, although they were always
slightly stronger for fatness predicting change in PA than
for PA predicting change in fatness (eg, BMI-SDS 7 years vs
MVPA 710 years: r=0.05, p=0.2; MVPA 7 years vs BMISDS 710 years: r=0.02, p=0.7; WC-SDS 7 years vs MVPA
710 years: r=0.07, p=0.2; MVPA 7 years vs WC-SDS 710
years: r=0.02, p=0.7).

DISCUSSION
Principal findings
This study con rms the inverse relationship between PA and
BF% reported previously by others.9 10 It goes further, however, and suggests that this relationship is dominated by the
impact of fatness on future activity rather than activity on
future fatness. The data were consistent from year to year and
in both sexes, and we believe that this is the rst evidence to
suggest direction of causality between fatness and activity in
children.

Strengths and weaknesses

Ours is not an intervention study but uses time to imply the
direction of causality. Importantly, the primary outcome
measures were both obtained using objective techniques.
Actigraph accelerometers and DEXA technology are considered criterion methods for measuring PA and BF%, respectively. 22 24 DEXA distinguishes fat from lean tissue and
reports true adiposity (BF%). BMI does not make the distinction, which is crucial because PA could readily increase lean/
muscle tissue. The lack of distinction between fat and lean
may explain why the associations between PA and BMI in
this study were weaker than those between PA and BF%.
The measurement of BF% is a more precise measure than that
of PA, and this could have contributed to our ndings. When
the less precise measure (PA) is the explanatory variable and
the more precise measure (BF%) is the outcome, the effect
size could underestimate the true effect. The cohort represents an exclusively urban population (98% of whom are
Caucasian) from a single location, which may limit its generalisability. A nal sample size of just >200 children may not
be considered large by previous cross-sectional standards,
but cross-sectional studies cannot address the question of
causality. The present study was longitudinal, and the ndings regarding causality are considered robust because they
were shown to be consistent across six pairs of temporal
relationships. Furthermore, although the nal sample of
n=202 represents only 66% of the original cohort recruited
4 of 6

at age 5 years, they were considered representative given

that their BMI and PA levels at recruitment were no different
from those of the 105 children excluded (BMI p=0.4, MVPA
p=0.2). Energy consumption is a notoriously unreliable measure in primary school children and could not be ruled out as
a possible confounder. The study did, however, measure food
choice by means of a food frequency questionnaire, but it
had no impact on the PA versus fatness relationship and was
not associated with either variable (p>0.5).

Strengths and weaknesses in relation to other studies

The literature contains a mix of studies addressing the relationship between PA and body mass. Some involve children,
and others involve only adults. Some report BMI alone, and
others report body composition, whereas some use subjective
and others use objective measures to do so. Some are observational, and others are interventional. Crucially, some examine
both directions of causality; others examine only one.
Four other longitudinal studies have exploited temporal relationships to examine causality in both directions
between PA and body mass, but only in adults.1215 All four
found that a higher body mass/fat consistently increased
the odds of becoming sedentary, whereas being sedentary
rarely increased the odds of becoming obese.1214 Although
three of the four studies involved large sample sizes (ranging from 2500 to 5500) and long follow-up periods (1025
years), all three nevertheless measured BMI rather than fatness and recorded PA by questionnaire, making it difcult
to exclude reporting bias as a possible confounder. Ekelund
and colleagues,15 on the other hand, recorded minute-byminute heart rate objectively over four consecutive days in
400 middle-aged adults. Body weight, BMI, girth and fat (by
bio-impedance) all predicted sedentary time 6 years later (all
p0.005), whereas sedentary time did not predict future body
weight, BMI, girth or fat (all p>0.05). Only one study has
measured activity (accelerometry) and fatness (DEXA) at two
time points in children. 25 Riddoch and colleagues reported
a small inverse association between activity at 12 years and
fatness at 14 years but did not analyse the reverse association between fatness at 12 years and activity at 14 years and
were, therefore, unable to determine the dominant direction
of causality.
A recent meta-analysis of 12 randomised controlled trials
(n>8000; average duration approximately 18 months) showed
that school-based PA interventions had no impact on BMI
(mean difference 0.01 kg/m 2; 95% CI 0.14 to 0.14) or BF%. 26
The authors concluded that there is evidence to suggest that
reduced PA may be a downstream effect of obesity. There is
only one experimental trial, however, that has measured the
response of activity to change in weight. In a sample of 22
adults, Levine and colleagues27 showed that a gain of 2.8 kg
in BF% (achieved by an 8-week overfeeding intervention)
decreased the distance walked by 1.5 miles/day (p<0.001).
Wareham and colleagues11 reviewed 11 intervention studies
that examined the response of body composition to PA (but
not PA to body composition) in children. Benet was reported
in just three.11 Of those, only one could attribute the effect to
exercise, as the interventions used in the other two involved
diet and exercise combined. The authors commented that
several of the trials that failed to show improvement in body
composition nevertheless recorded measurable increases in
PA. This was also the case in a recent randomised controlled
trial involving 134 overweight preschool children in Glasgow,
UK. 28 The 6-month intervention increased levels of objectively

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Original article
measured total PA (p<0.01) but had no impact on measures of
body mass or girth (both p~0.4).
Whereas neither the natural variation in PA among children
nor attempts to increase the amount appear to inuence the
fatness of children, PA nevertheless has a demonstrable benet on metabolic health. Our own published data suggest that
PA at the government-recommended level is associated with
dynamic improvements in metabolic health over time, even
in the absence of a change in BMI or body composition. 29 A
further review by Wareham and colleagues30 reported on 13
PA-based interventions in children, 11 of which showed a
reduction of insulin resistance levels.

CONCLUSIONS

Meaning of the study

Funding This report from the EarlyBird Diabetes Study was funded by the Bright
Futures Trust, Diabetes UK, Smiths Charity, the Child Growth Foundation, the
Diabetes Foundation, the Beatrice Laing Trust, Abbott, Astra-Zeneca, GSK, Ipsen
and Roche. None of the sources funding this study had any involvement in the
study design, collection or analysis of data, interpretation of findings or writing of
the manuscript.

There is no disputing the inverse association between PA and

BF%. However, the present study suggests reverse causality
as a plausible explanation for the failure of public health and
school-based interventions promoting PA in children consistently to reduce BMI or other measures of BF%. Authors
often speculate that their PA component was not sufciently
intense and intuitively recommend that future studies should
provide more. Our ndings suggest that rather than giving
children ever-increasing doses of PA, we should rst question
the basic paradigm that more PA leads to less fat. If childhood
fatness is not the result of physical inactivity, the implication may be that excess energy intake underlies fatness and
inactivity.

Possible explanations
We do not know why fatter children should be less active,
but psychological and physiological explanations appear to
be plausible. A review by Sallis and colleagues 31 showed that
in three of seven studies, perceived body image was related
to PA in adolescents. It is possible that overweight children
perceive their body image negatively and, as a result, choose
not to participate in sports and exercise. Several physiological
reasons are discussed in a recent review by Shultz and colleagues. 32 The authors suggest that exercise can cause musculoskeletal pain in overweight children. They imply that
the extra energy costs of moving a greater body mass would
cause breathlessness/fatigue sooner during exercise than for
a normal-weight child. These symptoms may be due to the
lower tness of the fatter child or associated with mitochondrial dysfunction. There is emerging evidence to suggest
that excess BF% and the insulin resistance associated with it
may lead to mitochondrial dysfunction. 33 Mitochondria are
responsible for delivering aerobic energy, crucial to muscle
tness. Failure to supply energy aerobically at the rate it is
needed leads to the accumulation of lactate, causing muscle discomfort and limiting tolerance to intense muscular
effort.

Unanswered questions and future research

Further research is required in children to test this reverse
causality more formally with experimental trials. If our ndings are replicated, future research should aim to provide a
better understanding of why fatness leads to inactivity but
inactivity does not lead to fatness. It is still not clear what
type of intervention is the most likely to succeed in preventing childhood obesity. However, given the relative success that
dietary interventions have had in improving BMI, 34 future
intervention studies should, perhaps, focus more on reducing
energy intake than on increasing energy expenditure.

The image of the couch-potato child who is obese because

he is sedentary runs deep in Western consciousness. However,
the possibility that the reverse obtains, that his fatness is the
cause rather than the result of his inactivity, has far-reaching
implications. Although there may be many benets to PA,
the ndings of this study, coupled with the limited success of
PA interventions aimed at improving BMI, imply that public
health strategies may need to target energy intake to curb the
year-on-year rise in childhood obesity.
Acknowledgements The authors thank Karen Brookes and Val Morgan for their
assistance with the data collection and Sharan Griffin for operating the DEXA
machine.

Competing interests None.

Contributors The authors have contributed the following and have seen and
approved the final version of this article. BSM, child health statistician: data entry,
analysis and writing. JH, child health statistician: data entry and analysis. ANJ,
research nurse: data collection. LDV, coordinator of the EarlyBird study: writing.
WH, University lecturer in statistics: statistical advice and analysis. TJW, director
of the EarlyBird study: writing.
Ethical approval Ethical approval was obtained from the Plymouth local research
ethics committee (South and West Devon Health Authority) in 1999. Informed
consent and assent were obtained from parents and children, respectively.
Provenance and peer review Not commissioned; externally peer reviewed.

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Metcalf BS, Hosking J, Jeffery AN, et al. Arch Dis Child (2010). doi:10.1136/adc.2009.175927

Downloaded from adc.bmj.com on April 21, 2011 - Published by group.bmj.com

Fatness leads to inactivity, but inactivity

does not lead to fatness: a longitudinal
study in children (EarlyBird 45)
B S Metcalf, J Hosking, A N Jeffery, et al.
Arch Dis Child published online June 23, 2010

doi: 10.1136/adc.2009.175927

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